High retinoid X receptor expression in JEG‐3 choriocarcinoma cells: Involvement in cell function modulation by retinoids
Identifieur interne : 004849 ( Main/Merge ); précédent : 004848; suivant : 004850High retinoid X receptor expression in JEG‐3 choriocarcinoma cells: Involvement in cell function modulation by retinoids
Auteurs : Jean Guibourdenche [France] ; Sylvie Roulier [France] ; Cécile Rochette-Egly [France] ; Danièle Evain-Brion [France]Source :
- Journal of Cellular Physiology [ 0021-9541 ] ; 1998-09.
Abstract
Retinoic acid (RA) is an important mediator of cell differentiation. It stimulates hCG secretion by JEG‐3 choriocarcinoma cells in vitro after a time lag. The first aim of this study was to characterize which types of retinoid receptors (RARs and RXRs) are present in JEG‐3 cells. Using Western blot analysis and immunocytochemistry with specific antibodies as well as Northern blot analysis, we found that JEG‐3 cells expressed RARα and RXRα, the latter being the predominant receptor. We then analyzed the action on cell proliferation and hCG secretion of the physiological retinoids all‐trans RA (RA) and 9 cis RA as well as synthetic retinoids with specific affinity for RARα and RXRα. All these retinoids were potent inhibitors of cell growth, maximal inhibition (72 ± 2%) being observed after 4 days of treatment with Ro 25, a RXRα specific ligand. Within 24 h, 9 cis RA and Ro 25 stimulated hCG secretion, and maximal stimulation (1,472 ± 10%) occurred at 48 h with the RXRα‐specific ligand. The RARα‐specific ligand also stimulated hCG secretion but to a lower extend and after a delay of 48 h. These results suggest a predominant role of RXRα in mediating the biological effects of retinoids on JEG‐3 cells and the possible induction by RA itself of the metabolic pathway leading to 9 cis RA. J. Cell. Physiol. 176:595–601, 1998. © 1998 Wiley‐Liss, Inc.
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DOI: 10.1002/(SICI)1097-4652(199809)176:3<595::AID-JCP16>3.0.CO;2-Z
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Cell. Physiol.</title><idno type="ISSN">0021-9541</idno><idno type="eISSN">1097-4652</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1998-09">1998-09</date><biblScope unit="volume">176</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="595">595</biblScope><biblScope unit="page" to="601">601</biblScope></imprint><idno type="ISSN">0021-9541</idno></series><idno type="istex">111C6403133F551893FB1C5394DE2D584D80118B</idno><idno type="DOI">10.1002/(SICI)1097-4652(199809)176:3<595::AID-JCP16>3.0.CO;2-Z</idno><idno type="ArticleID">JCP16</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0021-9541</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Retinoic acid (RA) is an important mediator of cell differentiation. It stimulates hCG secretion by JEG‐3 choriocarcinoma cells in vitro after a time lag. The first aim of this study was to characterize which types of retinoid receptors (RARs and RXRs) are present in JEG‐3 cells. Using Western blot analysis and immunocytochemistry with specific antibodies as well as Northern blot analysis, we found that JEG‐3 cells expressed RARα and RXRα, the latter being the predominant receptor. We then analyzed the action on cell proliferation and hCG secretion of the physiological retinoids all‐trans RA (RA) and 9 cis RA as well as synthetic retinoids with specific affinity for RARα and RXRα. All these retinoids were potent inhibitors of cell growth, maximal inhibition (72 ± 2%) being observed after 4 days of treatment with Ro 25, a RXRα specific ligand. Within 24 h, 9 cis RA and Ro 25 stimulated hCG secretion, and maximal stimulation (1,472 ± 10%) occurred at 48 h with the RXRα‐specific ligand. The RARα‐specific ligand also stimulated hCG secretion but to a lower extend and after a delay of 48 h. These results suggest a predominant role of RXRα in mediating the biological effects of retinoids on JEG‐3 cells and the possible induction by RA itself of the metabolic pathway leading to 9 cis RA. J. Cell. Physiol. 176:595–601, 1998. © 1998 Wiley‐Liss, Inc.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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